Pharmacodynamics describes how drugs produce effects in the body. Drugs act by binding to receptors, with higher affinity drugs binding more strongly as indicated by a lower Kd value. The dose-response curve plots the response achieved at different drug doses or concentrations, with the EC50 representing the dose/concentration that produces 50% of the maximum response. Plotting dose-response curves using log scales provides a sigmoidal shape that is easier to interpret, particularly at lower doses near the EC50.
Pharmacodynamics for Medical Students Part 2/3 by Dr. William K Limlim2010
Potency refers to the concentration or dose of a drug needed to produce a certain response level, usually 50% response. Efficacy refers to the maximum response a drug can produce when all receptors are occupied. A full agonist produces maximal response at receptor saturation while a partial agonist produces submaximal response. An antagonist binds receptors but produces no effect, instead blocking the effect of an agonist. Reversible antagonists dissociate from receptors while irreversible antagonists form covalent bonds and cannot dissociate.
The document discusses key concepts related to how ligands bind to proteins and receptors. It defines important terms like:
1) Equilibrium dissociation constant (Keq), which represents the concentration of ligand that occupies 50% of receptor sites. Keq is inversely related to affinity.
2) Potency, which refers to the concentration of a drug needed to produce a given effect. It is determined by receptor affinity.
3) Efficacy, which represents a drug's ability to induce a physiological response through a receptor. Full agonists elicit the maximum response while partial agonists have lower efficacy.
Mechanism of action of drugs can occur through various pathways including biochemical, physiological, physical, chemical, enzymatic, and receptor-mediated actions. Drugs can act through membrane-bound receptors by binding with varying affinity and efficacy, and can cause effects as agonists, antagonists, partial agonists, or inverse agonists. Factors like dosage, drug potency, efficacy, interactions, tolerance, and individual patient characteristics influence a drug's effects.
This document contains information on general pharmacology principles including pharmacokinetics, pharmacodynamics, and dose-response relationships. It discusses [1] how drugs interact with receptors according to the law of mass action and receptor occupancy theory, [2] factors that influence dose-response curves including efficacy, potency, and antagonism, and [3] the relationship between therapeutic effects and toxic effects as characterized by the therapeutic index. Additional study resources on these topics are provided.
This document summarizes key concepts in pharmacodynamics from a third semester pharmaceutical sciences group project. It defines pharmacodynamics as how drugs act on the body and influence the magnitude of response based on drug concentration. Most drugs exert their effects by interacting with receptors, and substances that can bind receptors and produce biological responses are called agonists. The relationship between drug concentration and response is shown using drug response curves, where efficacy is the maximum response and potency is the amount needed to produce the maximum effect, such as Candesartan being more potent than Ibesartan due to its lower dose range.
Here are the matches between the pharmacologic terms and their definitions:
1. Efficacy - C) This is the maximal response obtainable by a drug treatment
2. Potency - E) This is the amount of drug required to produce a desired effect
3. Tolerance - A) Decreased response to the same dose of the drug.
4. Therapeutic index - D) This is the ratio of the toxic dose to the therapeutic dose
5. Intolerance - B) When the antagonist is suddenly withdrawn, severe reaction occurs in the form of rebound or withdrawal effects
The presentation gives you a bird eye's view regarding basics of PK-PD modeling, its applications, types, limitations and various softwares used for the same.
This document discusses how various factors can modify the effects of drugs in patients. It describes how genetics, race, diet, environment, psychological factors, and concurrent diseases or medications can influence pharmacokinetic and pharmacodynamic processes. Specific examples are given of genetic polymorphisms that affect drug metabolism by enzymes like CYP2C9 and CYP2D6. It also explains concepts like tolerance, drug-drug interactions, receptor antagonism, and how conditions like liver or kidney disease can impact drug handling in the body. The lecturer concludes that considering these modifying factors is important for selecting appropriate drugs and doses for each individual patient.
Pharmacodynamics for Medical Students Part 2/3 by Dr. William K Limlim2010
Potency refers to the concentration or dose of a drug needed to produce a certain response level, usually 50% response. Efficacy refers to the maximum response a drug can produce when all receptors are occupied. A full agonist produces maximal response at receptor saturation while a partial agonist produces submaximal response. An antagonist binds receptors but produces no effect, instead blocking the effect of an agonist. Reversible antagonists dissociate from receptors while irreversible antagonists form covalent bonds and cannot dissociate.
The document discusses key concepts related to how ligands bind to proteins and receptors. It defines important terms like:
1) Equilibrium dissociation constant (Keq), which represents the concentration of ligand that occupies 50% of receptor sites. Keq is inversely related to affinity.
2) Potency, which refers to the concentration of a drug needed to produce a given effect. It is determined by receptor affinity.
3) Efficacy, which represents a drug's ability to induce a physiological response through a receptor. Full agonists elicit the maximum response while partial agonists have lower efficacy.
Mechanism of action of drugs can occur through various pathways including biochemical, physiological, physical, chemical, enzymatic, and receptor-mediated actions. Drugs can act through membrane-bound receptors by binding with varying affinity and efficacy, and can cause effects as agonists, antagonists, partial agonists, or inverse agonists. Factors like dosage, drug potency, efficacy, interactions, tolerance, and individual patient characteristics influence a drug's effects.
This document contains information on general pharmacology principles including pharmacokinetics, pharmacodynamics, and dose-response relationships. It discusses [1] how drugs interact with receptors according to the law of mass action and receptor occupancy theory, [2] factors that influence dose-response curves including efficacy, potency, and antagonism, and [3] the relationship between therapeutic effects and toxic effects as characterized by the therapeutic index. Additional study resources on these topics are provided.
This document summarizes key concepts in pharmacodynamics from a third semester pharmaceutical sciences group project. It defines pharmacodynamics as how drugs act on the body and influence the magnitude of response based on drug concentration. Most drugs exert their effects by interacting with receptors, and substances that can bind receptors and produce biological responses are called agonists. The relationship between drug concentration and response is shown using drug response curves, where efficacy is the maximum response and potency is the amount needed to produce the maximum effect, such as Candesartan being more potent than Ibesartan due to its lower dose range.
Here are the matches between the pharmacologic terms and their definitions:
1. Efficacy - C) This is the maximal response obtainable by a drug treatment
2. Potency - E) This is the amount of drug required to produce a desired effect
3. Tolerance - A) Decreased response to the same dose of the drug.
4. Therapeutic index - D) This is the ratio of the toxic dose to the therapeutic dose
5. Intolerance - B) When the antagonist is suddenly withdrawn, severe reaction occurs in the form of rebound or withdrawal effects
The presentation gives you a bird eye's view regarding basics of PK-PD modeling, its applications, types, limitations and various softwares used for the same.
This document discusses how various factors can modify the effects of drugs in patients. It describes how genetics, race, diet, environment, psychological factors, and concurrent diseases or medications can influence pharmacokinetic and pharmacodynamic processes. Specific examples are given of genetic polymorphisms that affect drug metabolism by enzymes like CYP2C9 and CYP2D6. It also explains concepts like tolerance, drug-drug interactions, receptor antagonism, and how conditions like liver or kidney disease can impact drug handling in the body. The lecturer concludes that considering these modifying factors is important for selecting appropriate drugs and doses for each individual patient.
Introduction to pharmacology and drug metabolismLuke Lightning
This document provides an introduction to the topics that will be discussed in a pharmacology lecture, including quantitative drug-receptor interactions, mechanisms of drug action, factors affecting drug effects, and absorption, distribution, metabolism, and excretion of drugs. The introduction defines pharmacology as the study of interactions between chemicals and biological systems, with a focus on how drugs work and are processed by the body. Key concepts covered include drug-receptor binding, concentration-response curves, receptor affinity and potency, agonists and antagonists, and time-action profiles of drugs.
The document discusses pharmacodynamics, which is the study of how drugs produce effects on living individuals. It explains that drug activity is measured by the physiological response produced, with more active drugs producing greater responses. Drug actions can be identified by their effects on stimulation, depression, irritation, or chemotherapy. Examples are given such as caffeine stimulating cortical activity and barbiturates depressing the central nervous system.
The document discusses various concepts related to pharmacology including dose-response relationships, drug potency and efficacy, therapeutic index, and factors that can influence drug response. It describes the graded and quantal types of dose-response curves and defines potency as the amount of drug required to produce a desired response. Therapeutic index is defined as the ratio of lethal to effective doses. The document also discusses how drug responses can be increased or decreased through summation, synergism, potentiation, and antagonism. Multiple factors are described that can affect drug response including route of administration, presence of other drugs, accumulation, and patient-related factors.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their effects. It describes how drugs can have therapeutic or adverse effects by stimulating, depressing, or replacing certain processes. The main targets of drugs are receptors, ion channels, enzymes, and transporter proteins. Receptors are sites that recognize signals and initiate responses. The document outlines different types of receptors like G-protein coupled, ion channel, enzyme, and nuclear receptors. It also discusses concepts like agonists, antagonists, efficacy, potency, dose-response curves, therapeutic index, and synergistic or antagonistic drug interactions.
The document provides an overview of pharmacodynamics, which is how drugs act on the body. It discusses drug receptor interactions including agonists that activate receptors, antagonists that block receptors, and partial agonists that partially activate receptors. It also covers non-receptor mechanisms of drug action such as effects on enzymes. The time and dose responses of drugs are described, as well as factors affecting drug activity like absorption, distribution, metabolism and excretion.
This document discusses pharmacodynamics concepts including graded dose response curves, potency, efficacy, therapeutic index, and types of antagonism. Graded dose response curves plot the magnitude of drug responses against increasing doses to determine efficacy, potency, and therapeutic index. Potency refers to the amount of drug needed to produce an effect, while efficacy refers to the magnitude of response. Therapeutic index is the ratio of lethal dose 50 (LD50) to effective dose 50 (ED50), and indicates a drug's safety margin. Antagonism can be chemical, physiological, pharmacological (competitive or noncompetitive), or biochemical in nature.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It describes different types of drug actions including local, systemic, and reflex actions. The mechanisms of drug action include effects on receptors as agonists, antagonists, or partial agonists. Other mechanisms are physical, chemical, interference with cell division or metabolic pathways, inhibition of enzymes, and effects on ion channels. Adverse effects are also discussed, including allergies, idiosyncrasies, side effects, overdose effects, tolerance, iatrogenic diseases, secondary effects, teratogenicity, drug dependence, and cytotoxic reactions.
THIS PPT INCLUDE PHARMACODYNAMICS AND THIS PPT IS VERY USEFUL FOR (MBBS,BDS ) STUDENTS ,POSTGRADUATE STUDENT (MD,MDS,Phd) STUDENTS TO UNDERSTAND PHARMACODYNAMICS.
Outcomes:
Students must be able to demonstrate knowledge of pharmacodynamics under the following headings:
• Definition
• Structurally specific drugs
• Structurally non-specific drugs
• Receptor binding
• Agonists and antagonists
• Intracellular receptors
• Enzyme receptors
• Transport carrier receptors
• Neurotransmitters
This document discusses pharmacodynamics and drug receptors. It defines pharmacodynamics as the study of pharmacological drug effects and mechanisms of action. The objectives are to understand drug-target cell interactions and characterize a drug's full scope and sequence of action, providing a basis for rational therapeutic use and new drug development. It describes different types of drug receptors, including ligand-gated ion channels, G-protein coupled receptors, and intracellular receptors. It also discusses concepts such as agonists, antagonists, and partial agonists that act on receptors to elicit responses or block responses.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
This document provides an overview of pharmacodynamics, which is the study of how drugs act on the body. It discusses key topics including:
- Mechanisms of drug action like agonism, antagonism, and efficacy
- Where drugs can bind in the body, primarily enzymes, ion channels, transporters, and receptors
- The four main families of receptors - ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors
- Concepts of dose response relationships, therapeutic indices, and the development of drug tolerance over time.
In summary, the document outlines fundamental principles of pharmacodynamics and how drugs interact with the body at a molecular level.
Pharmacodynamics is the study of what drugs do to the body, including their mechanisms of action, pharmacological effects, and adverse effects. Drugs can act through various mechanisms including stimulation, depression, irritation, replacement, cytotoxicity, and interactions with receptors, enzymes, ion channels, antibodies, and transporters. Adverse drug reactions can be predictable based on a drug's pharmacological properties or unpredictable idiosyncratic reactions. Predictable reactions include side effects, secondary effects, toxicity, and iatrogenic disease, while unpredictable reactions include allergies and idiosyncrasies.
This document discusses pharmacodynamics in anesthesia. It describes how drugs affect the body through mechanisms of action, drug-receptor interactions, and dose-response relationships. Factors like age, genetics, disease states can impact pharmacodynamics. Drugs act through receptor-mediated actions, with receptors on cell membranes determining effects. Receptors include ion channels, G-protein coupled receptors, and those activating protein kinases or transcription. The efficacy and potency of drugs are also discussed in relation to agonists, antagonists, competitive vs. non-competitive antagonism. Therapeutic indices compare median effective and toxic doses. Pharmacodynamics are affected by patient factors and drug properties.
Pharmacokinetics & Pharmacodynamic models, Tolerance, Hypersensitivity responseZulcaif Ahmad
This document discusses pharmacokinetics and pharmacodynamics concepts. It defines pharmacokinetics as the study of what the body does to a drug and pharmacodynamics as the study of what a drug does to the body. It describes several pharmacodynamic models including linear, log-linear, Emax, and sigmoid Emax models. It also discusses indirect response models, signal transduction models, tolerance models, and non-steady state models. Finally, it provides an overview of hypersensitivity types including type I-IV reactions.
The document discusses pharmacodynamics and how drugs act on the body. It describes how most drugs bind to receptors and the different types of receptors that exist. It explains drug-receptor binding kinetics using equations and graphs of dose-response curves. Different types of drugs are described like agonists that activate receptors, and antagonists that block receptor activation. The key signaling pathways of receptor activation are also summarized.
Pharmacodynamics is the study of how drugs act on the body and examines the biochemical and physiologic effects of drugs. It focuses on the drug's effects on cells and tissues. There are three main ways drugs can exert their effects: receptor interactions, enzyme interactions, and nonspecific interactions. The goal of drug therapy is to produce a therapeutic effect, while minimizing adverse effects. Drug response is monitored to evaluate therapeutic effects and detect undesirable side effects or toxicity.
This document discusses the importance of understanding the mechanism of drug action. It explains that pharmacodynamics is the study of how drugs work in the body and affect it biochemically and physiologically. Understanding these mechanisms is important for several reasons: 1) It helps build trust between patients and their doctors by allowing doctors to explain how the drug is working, 2) Patients who understand their treatment are more likely to participate in managing their disease, and 3) Knowing the mechanisms increases doctors' confidence that drugs are being used appropriately and helps avoid interactions and adverse effects.
Pharmacodynamics is the study of how drugs act on the body and biological system, including receptor interactions and mechanisms of action. Most drugs act by binding to receptors, and spare receptors allow a maximal response even when not all receptors are occupied, as only a portion need to be bound. Agonists activate receptors to produce a response, with full agonists having maximal efficacy and partial agonists having less efficacy than full agonists. Antagonists block the action of agonists without activating the receptors themselves.
The document discusses the law of mass action and binding of drugs to receptors. It describes how drug-receptor binding occurs at a rate dependent on drug and receptor concentrations. The dissociation constant (KD) represents the equilibrium between bound and unbound states. The affinity (KA) is the inverse of KD. A saturation curve shows half of receptors will be occupied when drug concentration equals KD.
The document discusses the law of mass action in pharmacology. It describes how drugs bind to receptors at a rate dependent on the drug and receptor concentrations. The dissociation constant (KD) represents the equilibrium between bound and unbound states. The affinity (KA) is the inverse of KD. A saturation curve shows the relationship between drug concentration and receptor occupancy.
Introduction to pharmacology and drug metabolismLuke Lightning
This document provides an introduction to the topics that will be discussed in a pharmacology lecture, including quantitative drug-receptor interactions, mechanisms of drug action, factors affecting drug effects, and absorption, distribution, metabolism, and excretion of drugs. The introduction defines pharmacology as the study of interactions between chemicals and biological systems, with a focus on how drugs work and are processed by the body. Key concepts covered include drug-receptor binding, concentration-response curves, receptor affinity and potency, agonists and antagonists, and time-action profiles of drugs.
The document discusses pharmacodynamics, which is the study of how drugs produce effects on living individuals. It explains that drug activity is measured by the physiological response produced, with more active drugs producing greater responses. Drug actions can be identified by their effects on stimulation, depression, irritation, or chemotherapy. Examples are given such as caffeine stimulating cortical activity and barbiturates depressing the central nervous system.
The document discusses various concepts related to pharmacology including dose-response relationships, drug potency and efficacy, therapeutic index, and factors that can influence drug response. It describes the graded and quantal types of dose-response curves and defines potency as the amount of drug required to produce a desired response. Therapeutic index is defined as the ratio of lethal to effective doses. The document also discusses how drug responses can be increased or decreased through summation, synergism, potentiation, and antagonism. Multiple factors are described that can affect drug response including route of administration, presence of other drugs, accumulation, and patient-related factors.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their effects. It describes how drugs can have therapeutic or adverse effects by stimulating, depressing, or replacing certain processes. The main targets of drugs are receptors, ion channels, enzymes, and transporter proteins. Receptors are sites that recognize signals and initiate responses. The document outlines different types of receptors like G-protein coupled, ion channel, enzyme, and nuclear receptors. It also discusses concepts like agonists, antagonists, efficacy, potency, dose-response curves, therapeutic index, and synergistic or antagonistic drug interactions.
The document provides an overview of pharmacodynamics, which is how drugs act on the body. It discusses drug receptor interactions including agonists that activate receptors, antagonists that block receptors, and partial agonists that partially activate receptors. It also covers non-receptor mechanisms of drug action such as effects on enzymes. The time and dose responses of drugs are described, as well as factors affecting drug activity like absorption, distribution, metabolism and excretion.
This document discusses pharmacodynamics concepts including graded dose response curves, potency, efficacy, therapeutic index, and types of antagonism. Graded dose response curves plot the magnitude of drug responses against increasing doses to determine efficacy, potency, and therapeutic index. Potency refers to the amount of drug needed to produce an effect, while efficacy refers to the magnitude of response. Therapeutic index is the ratio of lethal dose 50 (LD50) to effective dose 50 (ED50), and indicates a drug's safety margin. Antagonism can be chemical, physiological, pharmacological (competitive or noncompetitive), or biochemical in nature.
This document discusses pharmacodynamics, which is the study of how drugs act on the body and their mechanisms of action. It describes different types of drug actions including local, systemic, and reflex actions. The mechanisms of drug action include effects on receptors as agonists, antagonists, or partial agonists. Other mechanisms are physical, chemical, interference with cell division or metabolic pathways, inhibition of enzymes, and effects on ion channels. Adverse effects are also discussed, including allergies, idiosyncrasies, side effects, overdose effects, tolerance, iatrogenic diseases, secondary effects, teratogenicity, drug dependence, and cytotoxic reactions.
THIS PPT INCLUDE PHARMACODYNAMICS AND THIS PPT IS VERY USEFUL FOR (MBBS,BDS ) STUDENTS ,POSTGRADUATE STUDENT (MD,MDS,Phd) STUDENTS TO UNDERSTAND PHARMACODYNAMICS.
Outcomes:
Students must be able to demonstrate knowledge of pharmacodynamics under the following headings:
• Definition
• Structurally specific drugs
• Structurally non-specific drugs
• Receptor binding
• Agonists and antagonists
• Intracellular receptors
• Enzyme receptors
• Transport carrier receptors
• Neurotransmitters
This document discusses pharmacodynamics and drug receptors. It defines pharmacodynamics as the study of pharmacological drug effects and mechanisms of action. The objectives are to understand drug-target cell interactions and characterize a drug's full scope and sequence of action, providing a basis for rational therapeutic use and new drug development. It describes different types of drug receptors, including ligand-gated ion channels, G-protein coupled receptors, and intracellular receptors. It also discusses concepts such as agonists, antagonists, and partial agonists that act on receptors to elicit responses or block responses.
Receptor types, mechanism, receptor pharmacology, drug receptor interactions, theories of receptor pharmacology, spare receptors and new concepts like biased agonism
This document provides an overview of pharmacodynamics, which is the study of how drugs act on the body. It discusses key topics including:
- Mechanisms of drug action like agonism, antagonism, and efficacy
- Where drugs can bind in the body, primarily enzymes, ion channels, transporters, and receptors
- The four main families of receptors - ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, and nuclear receptors
- Concepts of dose response relationships, therapeutic indices, and the development of drug tolerance over time.
In summary, the document outlines fundamental principles of pharmacodynamics and how drugs interact with the body at a molecular level.
Pharmacodynamics is the study of what drugs do to the body, including their mechanisms of action, pharmacological effects, and adverse effects. Drugs can act through various mechanisms including stimulation, depression, irritation, replacement, cytotoxicity, and interactions with receptors, enzymes, ion channels, antibodies, and transporters. Adverse drug reactions can be predictable based on a drug's pharmacological properties or unpredictable idiosyncratic reactions. Predictable reactions include side effects, secondary effects, toxicity, and iatrogenic disease, while unpredictable reactions include allergies and idiosyncrasies.
This document discusses pharmacodynamics in anesthesia. It describes how drugs affect the body through mechanisms of action, drug-receptor interactions, and dose-response relationships. Factors like age, genetics, disease states can impact pharmacodynamics. Drugs act through receptor-mediated actions, with receptors on cell membranes determining effects. Receptors include ion channels, G-protein coupled receptors, and those activating protein kinases or transcription. The efficacy and potency of drugs are also discussed in relation to agonists, antagonists, competitive vs. non-competitive antagonism. Therapeutic indices compare median effective and toxic doses. Pharmacodynamics are affected by patient factors and drug properties.
Pharmacokinetics & Pharmacodynamic models, Tolerance, Hypersensitivity responseZulcaif Ahmad
This document discusses pharmacokinetics and pharmacodynamics concepts. It defines pharmacokinetics as the study of what the body does to a drug and pharmacodynamics as the study of what a drug does to the body. It describes several pharmacodynamic models including linear, log-linear, Emax, and sigmoid Emax models. It also discusses indirect response models, signal transduction models, tolerance models, and non-steady state models. Finally, it provides an overview of hypersensitivity types including type I-IV reactions.
The document discusses pharmacodynamics and how drugs act on the body. It describes how most drugs bind to receptors and the different types of receptors that exist. It explains drug-receptor binding kinetics using equations and graphs of dose-response curves. Different types of drugs are described like agonists that activate receptors, and antagonists that block receptor activation. The key signaling pathways of receptor activation are also summarized.
Pharmacodynamics is the study of how drugs act on the body and examines the biochemical and physiologic effects of drugs. It focuses on the drug's effects on cells and tissues. There are three main ways drugs can exert their effects: receptor interactions, enzyme interactions, and nonspecific interactions. The goal of drug therapy is to produce a therapeutic effect, while minimizing adverse effects. Drug response is monitored to evaluate therapeutic effects and detect undesirable side effects or toxicity.
This document discusses the importance of understanding the mechanism of drug action. It explains that pharmacodynamics is the study of how drugs work in the body and affect it biochemically and physiologically. Understanding these mechanisms is important for several reasons: 1) It helps build trust between patients and their doctors by allowing doctors to explain how the drug is working, 2) Patients who understand their treatment are more likely to participate in managing their disease, and 3) Knowing the mechanisms increases doctors' confidence that drugs are being used appropriately and helps avoid interactions and adverse effects.
Pharmacodynamics is the study of how drugs act on the body and biological system, including receptor interactions and mechanisms of action. Most drugs act by binding to receptors, and spare receptors allow a maximal response even when not all receptors are occupied, as only a portion need to be bound. Agonists activate receptors to produce a response, with full agonists having maximal efficacy and partial agonists having less efficacy than full agonists. Antagonists block the action of agonists without activating the receptors themselves.
The document discusses the law of mass action and binding of drugs to receptors. It describes how drug-receptor binding occurs at a rate dependent on drug and receptor concentrations. The dissociation constant (KD) represents the equilibrium between bound and unbound states. The affinity (KA) is the inverse of KD. A saturation curve shows half of receptors will be occupied when drug concentration equals KD.
The document discusses the law of mass action in pharmacology. It describes how drugs bind to receptors at a rate dependent on the drug and receptor concentrations. The dissociation constant (KD) represents the equilibrium between bound and unbound states. The affinity (KA) is the inverse of KD. A saturation curve shows the relationship between drug concentration and receptor occupancy.
Factors modifying drug action, efficacy & potencyBADAR UDDIN UMAR
1. The document discusses key concepts related to how drugs act including affinity, efficacy, potency, graded and quantal dose-response relationships.
2. It explains that affinity refers to a drug's tendency to bind receptors, efficacy is a drug's ability to produce a maximum response, and potency is the concentration needed to produce 50% of a drug's effect.
3. The document also discusses factors that modify drug action such as age, metabolism, and genetic factors. It emphasizes that drug potency determines dosage while efficacy impacts clinical effectiveness.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
This document describes key concepts related to dose-response relationships and drug interactions. It defines dose-response relationships and curves, and explains how drug potency, efficacy, selectivity, and therapeutic index are determined based on these curves. It also discusses how drugs can have synergistic or antagonistic effects when combined, including competitive and non-competitive receptor antagonism. The overall intent is to explain important pharmacological concepts for understanding how drug effects are produced at varying doses both alone and when administered together with other drugs.
The document discusses dose-response relationships, which relate the amount of a drug administered (dose) to its biological effect (response). It defines key terms like dose, response, dose-response curve, potency, efficacy, and therapeutic index. Dose-response curves can take different shapes depending on whether response is measured quantally or gradually, and can be used to determine a drug's potency, efficacy, and margin of safety between therapeutic and toxic doses.
Pharmacodynamics is the study of how drugs act on the body and biological system, including the receptors to which they bind, and their mechanisms of action and effects. Most drugs act by interacting with receptors, which are usually proteins, though some drugs can act without directly binding to receptors. The relationship between the dose level of a drug and its therapeutic effects or toxic side effects can be shown using dose-response curves and is important for understanding a drug's safety and efficacy.
Lecture Objectives:
After completion of the lecture, students will be able to:
• Describe Quantitatively describe the relationship between drug, receptor,
and the pharmacologic response.
• Explain why the intensity of the pharmacologic response increases with
drug concentrations and/or dose up to a maximum response.
• Describe relationship of dose to pharmacologic effect
Dose-Response Relationship:
A drug's pharmacological effect is determined by its concentration at the site of action, which is determined by the dose administered. Such a relationship is called 'dose-response relationship’.
The document discusses the relationship between the amount of drug in the body and its effect, known as the dose-effect relationship. It explains that this relationship is determined by several factors in a causal chain, including the dose of the drug, the concentration of drug at the target site, the formation of drug-receptor complexes, and the response. The relationship between drug concentration and receptor binding is nonlinear, which shapes the sigmoidal dose-effect curve. Blocking drugs can alter this curve depending on their mechanism of action. Population dose-response curves examine the quantal effects of drugs across individuals.
The document discusses dose-response curves and their significance. It explains that dose-response curves show the relationship between the dose of a drug administered and the intensity of response produced. A log dose-response curve becomes sigmoid shaped and allows comparison of drug potency. The position, slope and maximum effect of the curve provide information about a drug's potency, efficacy, safety, therapeutic index and window. Quantal and graded dose-response curves are used to assess different types of drug responses.
1. Pharmacodynamics is the study of how drugs act on the body, including their mechanisms of action.
2. Drugs primarily act by interacting with proteins like receptors, ion channels, enzymes, and transporters. They can also act physically or chemically.
3. Drugs can have stimulatory, depressant, replacement, or cytotoxic effects by interacting with enzymes, receptors, or through physical/chemical actions. The most common mechanism is receptor interaction.
Pharmacology I Pharmacodynamics III (DRC & combine effect of drug)Subhash Yende
This document discusses pharmacodynamics and the combined effects of drugs. It explains dose-response relationships and how drug potency and efficacy are determined based on the dose-response curve. The therapeutic index is defined as the ratio of lethal dose to effective dose. Drugs can have synergistic, additive, or antagonistic effects when used in combination. Synergism occurs when drug actions are facilitated while antagonism occurs when one drug decreases the action of another. The document provides examples of different types of combined drug effects.
- A dose response relationship describes how the magnitude of a drug's effect varies with increasing or decreasing doses. Dose response curves plot this relationship, with dose on the x-axis and response on the y-axis.
- There are two main types of dose response curves: graded/quantitative curves where response increases continuously with dose, and quantal/all-or-none curves where responses are binary above a threshold dose.
- The shape, slope, efficacy and potency of a dose response curve provide information about a drug's effects, safety, and relative potencies of similar drugs. Steep curves indicate higher potency while flatter curves suggest a drug has less impact over a range of doses.
bind to receptors and produce a response-
effects of various types
2. Antagonists
bind to receptors without producing a response and by occupying the receptors they prevent action of agonists.
branch of pharmacology dedicated to determine the fate of substances administ...adnan mansour
Pharmacokinetics (from Ancient Greek pharmakon "drug" and kinetikos "moving, putting in motion"; see chemical kinetics), sometimes abbreviated as PK, is a branch of pharmacology dedicated to determine the fate of substances administered to a living organism. The substances of interest include any chemical xenobiotic such as: pharmaceutical drugs, pesticides, food additives, cosmetics, etc. It attempts to analyze chemical metabolism and to discover the fate of a chemical from the moment that it is administered up to the point at which it is completely eliminated from the body. Pharmacokinetics is the study of how an organism affects a drug, whereas pharmacodynamics (PD) is the study of how the drug affects the organism. Both together influence dosing, benefit, and adverse effects, as seen in PK/PD models.
Pharmacokinetics (from Ancient Greek pharmakon "drug" and kinetikos "moving, putting in motion"; see chemical kinetics), sometimes abbreviated as PK, is a branch of pharmacology dedicated to determine the fate of substances administered to a living organism. The substances of interest include any chemical xenobiotic such as: pharmaceutical drugs, pesticides, food additives, cosmetics, etc. It attempts to analyze chemical metabolism and to discover the fate of a chemical from the moment that it is administered up to the point at which it is completely eliminated from the body. Pharmacokinetics is the study of how an organism affects a drug, whereas pharmacodynamics (PD) is the study of how the drug affects the organism. Both together influence dosing, benefit, and adverse effects, as seen in PK/PD models.
Design and optimizing of dosage regimen - pharmacology Areej Abu Hanieh
Drug therapy is initiated using a dosage regimen administered continuously or intermittently to achieve steady state concentrations. The regimen depends on factors like how rapidly steady state is needed. Steady state occurs when the rate of drug administration equals elimination, maintaining constant plasma levels. The goal is to refine regimens to provide maximum benefit with minimum adverse effects.
Similar to Pharmacodynamics for Medical Students Part 1/3 by Dr. WIlliam K Lim (20)
The chapter Lifelines of National Economy in Class 10 Geography focuses on the various modes of transportation and communication that play a vital role in the economic development of a country. These lifelines are crucial for the movement of goods, services, and people, thereby connecting different regions and promoting economic activities.
Gender and Mental Health - Counselling and Family Therapy Applications and In...PsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
How to Make a Field Mandatory in Odoo 17Celine George
In Odoo, making a field required can be done through both Python code and XML views. When you set the required attribute to True in Python code, it makes the field required across all views where it's used. Conversely, when you set the required attribute in XML views, it makes the field required only in the context of that particular view.
How to Setup Warehouse & Location in Odoo 17 InventoryCeline George
In this slide, we'll explore how to set up warehouses and locations in Odoo 17 Inventory. This will help us manage our stock effectively, track inventory levels, and streamline warehouse operations.
This presentation was provided by Racquel Jemison, Ph.D., Christina MacLaughlin, Ph.D., and Paulomi Majumder. Ph.D., all of the American Chemical Society, for the second session of NISO's 2024 Training Series "DEIA in the Scholarly Landscape." Session Two: 'Expanding Pathways to Publishing Careers,' was held June 13, 2024.
Level 3 NCEA - NZ: A Nation In the Making 1872 - 1900 SML.pptHenry Hollis
The History of NZ 1870-1900.
Making of a Nation.
From the NZ Wars to Liberals,
Richard Seddon, George Grey,
Social Laboratory, New Zealand,
Confiscations, Kotahitanga, Kingitanga, Parliament, Suffrage, Repudiation, Economic Change, Agriculture, Gold Mining, Timber, Flax, Sheep, Dairying,
A Visual Guide to 1 Samuel | A Tale of Two HeartsSteve Thomason
These slides walk through the story of 1 Samuel. Samuel is the last judge of Israel. The people reject God and want a king. Saul is anointed as the first king, but he is not a good king. David, the shepherd boy is anointed and Saul is envious of him. David shows honor while Saul continues to self destruct.
4. Pharmacology
Pharmacokinetics Pharmacodynamics
Adsorption * How does the drug
Distribution interact with the cell?
Metabolism * How does the drug
Excretion cause a therapeutic effect?
What the body does What the drug does
to the drug to the body
5. Pharmacology
Pharmacokinetics Pharmacodynamics
Adsorption * How does the drug
Distribution interact with the cell?
Metabolism * How does the drug
Excretion cause a therapeutic effect?
What the body does What the drug does
to the drug to the body
13. Concept of Receptor
Some drugs do not require a receptor for their effect:
e.g.
antacid: - changes pH of stomach
aspirin: - forms covalent bond with enzyme
kaolin: - adsorbs toxin in the gastrointestinal tract
15. Concept of Receptor
cell
Drug Molecules
Langley 1878:
‘Drug binds to a receptive substance on the cell’
(drugs must first bind to a receptor to produce their
action)
21. Main Families
of ReceptorsIon Channels
(open up for ions to pass)
G protein Coupled Receptors
(intracellular part of the receptor
activate or inhibit cellular proteins)
22. Main Families
of ReceptorsIon Channels
(open up for ions to pass)
G-protein Coupled Receptors
(intracellular part of the receptor
activate or inhibit cellular proteins)
Receptor Tyrosine Kinase
(phosphorylate intracellular proteins)
Intracellular Receptors
(enter nucleus,
promote gene transcription)
26. G-protein Coupled Receptor
Receptor
G proteins
MODERN DRUG DISCOVERY NOVEMBER 2004 p24-28
Receptor
G proteins
Inside
the
cell
Outside
the cell
Hormone
27. G-protein Coupled Receptor
Receptor
G proteins
MODERN DRUG DISCOVERY NOVEMBER 2004 p24-28
Inside
the cell
Outside
the cell
Activate or inhibit other proteins, leading to
final effect e.g. muscle contraction, enzyme
secretion, etc.
33. Drug-Receptor Binding
D = Drug R = Receptor
D + R DR Effect
Principle: Drug-receptor binding
follows the Law of Mass Action:
34. Drug-Receptor Binding
D = Drug R = Receptor
D + R DR Effect
Principle: Drug-receptor binding
follows the Law of Mass Action:
• D and R bind after they collide randomly
35. Drug-Receptor Binding
D = Drug R = Receptor
D + R DR Effect
Principle: Drug-receptor binding
follows the Law of Mass Action:
• D and R bind after they collide randomly
D + R DR
• After binding, D can dissociate from R
D + R DR
36. Drug-Receptor Binding
D = Drug R = Receptor
D + R DR Effect
At equilibrium, ( or )
association rate = dissociation rate
38. Drug-Receptor Binding
D + R DR
• At equilibrium, some of the D is binding to R
• If the number of R is constant,
then if D increases, DR also increases
D + R D R
D+ R DR
39. Drug Dose/Concentration &
Receptor Binding
D + R DR
Plot DR versus D:
100%
0
50%
DR ( %
of Receptor
bound to
Drug)
D (Drug Concentration)
40. Drug – Receptor binding experiment
Receptor (in cell membranes)
+
drug
Wait for equilibrium……
45. Drug Dose/Concentration &
Receptor Binding
D + R DR
Plot DR versus D:
100%
0
50%
DR ( %
of Receptor
bound to
Drug)
D (Drug Concentration)
46. Drug Concentration &
Receptor Binding
D + R DR
Plot a graph of DR against D:
D (Drug Concentration) [or amount]
DR ( %
of Receptor
bound to
Drug)
100%
0
50%
48. Drug Concentration &
Receptor Binding
D (conc)
B (% Bound)
• Equation: B (amt bound) Bmax . D
D + Kd
100
50
0
Rectangular
Hyperbolic
Curve
49. Drug Concentration &
Receptor Binding
D (conc)
B (% Bound)
• Equation: B (amt bound) Bmax . D
D + Kd
• Kd = dissociation constant
- concentration of drug when 50% of the
receptors are bound.
100
50
0
Rectangular
Hyperbolic
Curve
50. Drug Concentration &
Receptor Binding
D (conc)
B (% Bound)
• Equation: B (amt bound) Bmax . D
D + Kd
• Kd = A measure of affinity of drug for receptor
Every drug that can bind a receptor has a Kd value for
that receptor.
100
50
0
Rectangular
Hyperbolic
Curve
51. Drug Concentration &
Receptor Binding
D (conc)
B (% Bound)
• Equation: B (amt bound) Bmax . D
D + Kd
• Kd = A measure of affinity of drug for receptor
The higher the affinity, the smaller the Kd
100
50
0
Rectangular
Hyperbolic
Curve
56. Drug Concentration/Dose
& Receptor Binding
B
(% receptor
bound)
100
50
0
0 5 10 20 30 40
D (Drug conc) (mg/mL)
Drug A
Drug B
Kd (Drug A) = 10 mg/mL
Kd (Drug B) = 5 mg/mL
57. Drug Concentration/Dose
& Receptor Binding
B
(% receptor
bound)
100
50
0
0 5 10 20 30 40
D (Drug conc) (mg/mL)
Drug A
Drug B
Kd (Drug A) = 10 mg/mL
Kd (Drug B) = 5 mg/mL
The higher the affinity, the smaller the Kd
58. Drug Concentration/Dose
& Receptor Binding
B
(% receptor
bound)
100
50
0
0 5 10 20 30 40
D (Drug conc) (mg/mL)
Drug A
Drug B
Drug B has a higher affinity for the receptor than Drug A, so
Kd for drug B is smaller.
Kd (Drug A) = 10 mg/mL
Kd (Drug B) = 5 mg/mL
59. Drug Concentration/Dose
& Receptor Binding
• Kd = dissociation constant : concentration of
drug when 50% of the receptors are bound.
= A measure of affinity of drug for receptor
- The higher the affinity, the smaller the Kd
66. Drug Dose &
Response/Effect
D + R DR Response
(ED50)
ED50 (effective dose 50%) = drug dose that give 50% of
maximum response
Response
(% max)
Drug Dose
100
50
0
A ‘dose response curve’
67. Drug Dose &
Response/Effect
D + R DR Response
ED50 (effective dose 50%) or EC50 (effective conc
50%) =drug dose or conc giving 50% of max response
Response
(% max)
Drug Dose or Concentration
100
50
0
A ‘dose response curve’
68. Drug Dose &
Response/Effect
D + R DR Response
Every drug that can bind a receptor to produce a
response has a EC50 or ED50 value for that response
Response
(% max)
Drug Dose or Concentration
100
50
0
A ‘dose response curve’
72. Drug Dose & Response
Plotting response versus log dose (or log conc):
sigmoidal log-dose response curve
100
50
0
Log dose
Response
(% max)
• Most important type of graph in pharmacology:
• For comparing different drugs
-9 -8 -7 -6 -5 -4
74. Drug Dose & Response
100
50
0
Response
%
Response
%
[Drug Conc]
100
50
0
(arithmetic scale) (log scale)
Reasons to plot semi-log dose-response curves:
• Easier to interpret:
expands the scale at low concentrations
75. Drug Dose & Response
100
50
0
Response
%
Response
%
[Drug Conc]
100
50
0
(arithmetic scale) (log scale)
Reasons to plot semi-log dose-response curves:
• Easier to interpret:
expands the scale at low concentrations
76. Drug Dose & Response
100
50
0
Response
%
Response
%
[Drug Conc]
100
50
0
(arithmetic scale) (log scale)
Reasons to plot semi-log dose-response curves:
• Easier to interpret:
and compresses the scale at high concentrations.
77. Drug Dose & Response
100
50
0
Response
%
Response
%
[Drug Conc]
100
50
0
(arithmetic scale) (log scale)
Reasons to plot semi-log dose-response curves:
• Easier to interpret:
•Linear between 20 to 80% of maximal response
- the dose range of drugs most commonly studied
78. Summary
• Definition of pharmacodynamics
• Concept of receptor
• Concept of affinity of a drug for a receptor
• Drug binding curve: definition of Kd
• Dose response curve: definition of ED50(orEC50)
• Plotting log dose-response curves
79. • What is potency?
• What is efficacy?
• What is an agonist?
• What is an antagonist?
2013 contd good feedback as lecturer, mention during lect which curve get which data, in revision class show all wrong interpretation cos cannot get Kd from response curve etc. Made EOB SEQ on which drug higher affinity from this curve (its response curve) and which more potent/effic- 121 students- max 15 marks, 7 got either 1 or 0 mark.
Only 4 (3.3% of students) got 12 marks or more (able to say this curve cannot get affinity info: Yap Wen Nee, viviene jane, dylan harry, chai chang xian. Ave mark 5.4 (fail)
2013 45 min. no interaction, just give analogies- affinity for food, students bump into chairs, sit and stand. One asked is dose response related to michaelis menten enzyme kinetics- reaction rate v increases with substrate conc. Max is vmax, and substate conc for half Vmax is Km. http://medicaltextbooksrevealed.s3.amazonaws.com/files/11189-53.pdf ‘The same mathematical relationships that define how a drug (ligand) interacts with a receptor to elicit or diminish a biological response also governs the ways in which substrates (ligands) interact with enzymes to generate metabolic end products. In fact, the terms KD and Emax (ceiling effect) can easily be redefined as Km and Vmax, which you recall from Michaelis-Menten enzyme kinetics.’ ‘Dose – response curves and enzyme kinetics. These are the same. The familiar dose-response curves are based on the Michaelis – Menten model of enzyme substrate interaction’. http://www.frca.co.uk/article.aspx?articleid=101185. a dose response curve can obey first order Hill equation (Hill coefficient = 1) A first-order Hill function (means no cooperativity- binding of ligands are independent of each other’s binding) is sometimes called a Michaelis-Menten function).
‘The fact that dose-response curves varied so much made pharmacology different from biochemistry. The concentration of a drug which produced a half-maximum response from a tissue, EC50, was not constant: with powerful agonists a maximum response was produced from the activation of only a small proportion of receptors.‘http://www.pa2online.org/articles/?volume=1&issue=2. ‘So the dissociation constant is a measure of the affinity of the drug for its receptor, just like the Michaelis-Menten constant (Km) is a measure of the affinity of a substrate for its enzyme. At equilibrium, the reaction can also be expressed by this equation which takes the
same form as the Michaelis-Menten equation. ‘Drug concentration- effect relationship can be described by: 1) Michaelis-Menten equation for enzyme-substrate reaction’. So far can say if based on single site and no cooperative binding then dose response curve is similar to michelis menten where velocity become effect and EC50 is Km.
End lect can use class name list to read out names of 4 students to ask them define at next class what is potency, efficacy, agonist and antag.
A receptor can be any cellular macromolecule to which a drug binds to initiate its effect. Cellular proteins that are receptors for endogenous regulatory ligands (hormones,
growth factors, neurotransmitters) are the most important drug receptors. Other receptors include enzymes (e.g., acetylcholinesterase), transport proteins (e.g., Na+,K+-ATPase), structural proteins (e.g., tubulin), and nucleic acids.
When the relationship between receptor occupancy and response is linear, KD = EC50. If there is amplification between receptor occupancy and effect, such as if the receptor has catalytic activity when the receptor ligand is bound, then the EC50 lies to the left of the KD.
2012 50 min. student ask can binding curve also do semi log, and is binding curve same shape as response curve.- yes binding curve in log appear in lecture 2, will inform students there. In 3rd lect can give eg of real binding and response curve from journals, see same shape.
2011 had question why log scale is 1,10,100, 1000 – does log make scale increase very fast (aside from initial one to 3 is sparser and 3 to 10 is compressed)? (yes it increase exponential not arithmetical) And we say is log scale but never need to get antilog, just read off, though axis is officially log? (yes cos never took log, just plot on a scale with different intervals)
From the questions in ‘what else I want to know’ slips, some wonder how the binding/response expt is done so I put the binding expt pictorial in formative assessment
2010 45 min. supported by hard copy notes. if at end want to emphasise the impt of differentiate binding and effect curve then before show summary, show the diagram of drugs near the receptor with effect- put a dividing line and say again there are 2 different expt, 2 different part of the process, and first thing when see graph is ask what curve, then can know what info can get. Then I got 4 students to each read up on potency, effic, agonist and antag.
Concept of receptor and how to analyse D-R binding
How the drug at site of action produces an effect: receptor bind, quantitative analysis for comparing different drugs
Concept of receptor and how to analyse D-R binding
Note kinetic still occur after work at site, but it does mean dynamic cannot occur until drug arrive at site of action
How the drug at site of action produces an effect: receptor bind, quantitative analysis for comparing different drugs
Take a drug not just to metab and excrete it but cos you want it to act on body.
Take a drug not just to metab and excrete it but cos you want it to act on body.
Inhib cyclooxegenase which convert AA to PG, TX and Prostacyclin
Before showing the main types of receptor, would be clearer to explain that in general drug bind receptor which then activate downstream signals to amplify and generate the effect.
Before showing the main types of receptor, would be clearer to explain that in general drug bind receptor which then activate downstream signals to amplify and generate the effect.
Not just stand at door, come in, start the action
Receptors are types of doors, once activated, action starts
receptor for the epidermal growth factor (EGF) – receptor tyr kinase
ifn= interferon receptor- class II cytokine receptor family. The Janus (JAK) family tyrosine kinases Tyk2 and Jak1 are constitutively associated with the IFNAR1 and IFNAR2c receptor subunits, respectively. Ligand binding results in the phosphorylation and activation of Tyk2 and Jak1
Tnf receptor- TNF is a cytokine which may induce either cell proliferation or apoptosis. TNF binds TNF Receptors (TNFRs), which are members of a superfamily of proteins known as Death Receptors, resulting in receptor aggregation and recruitment of adapters (i.e., TRAF [TNF Receptor-Associated Factor] proteins) TNFR complex formation activates Caspase 8, the SAP Kinase pathway (dependent on recruitment of Daxx), and the NFκB pathway (which controls apoptosis versus proliferation).
Nicotinic cholinergic receptor
- Composed of 5 peptide subunits: 2α, 1β, 1γ, 1δ
Receptor on muscle fibre eg respiratory muscles- how does it contract. Nerve release NT bind to receptor.
The two binding sites for AcCho are nonidentical and can
be distinguished by differential binding of some competitive
antagonists. In particular, d-tubocurarine (TC) binds with
dissociation constants that differ by -100-fold
May need show more cascade and recoupling, else some wonder what is G doing
May need show more cascade and recoupling, else some wonder what is G doing
May need show more cascade and recoupling, else some wonder what is G doing
Affinity is bind with tenacity
Like all stand and move, but eyes close, move quietly so have random collisions.
randomly meet at party but after talk, can dissociate and meet others
there are some binding and others unbinding- so arrow in 2 direction, at equib, rate is equal. at any moment, some (not all) are bound
At first more DR formed. Later, more DR dissociate. At equib, rate is same.
Rate of nos sitting down is same as nos standing up from sitting.
Illus; 10am shopping centre open and number of people inside increases. Till 11am there is 100 inside though 30 enter from 11-12 yet only 100 total inside- cos 30 also leave- equib. But no matter how many inside (30, 50 then 100, majority are at one shop, the most popular one (MPH book, Guess jeans, CD,DVD, Nike shoes) then customer has highest affinity for that store. Lower affinity for other store and no affinity for certain store.
Collide = all move blindfold and no noise
Case of where nos of people of shopping centre the same though new one go in, cos some go out, and more will be at fav store- higher affinity
Till all receptors bound
Till all receptors bound
Can be dose or conc. Dose is what you give, conc is level in blood. More dose, more conc. Plot whichever
Can be dose or conc. Dose is what you give, conc is level in blood. More dose, more conc. Plot whichever
For ease just say receptor binding
If you bring in more student (eg 1000 student in this room of 100 chairs) eventually every chair will be occupied- 100% receptor bound.
Draw higher affinity plot to compare
Draw higher affinity plot to compare
Draw higher affinity plot to compare
Draw higher affinity plot to compare
Draw higher affinity plot to compare
Can you do this
Can you do this
What is kd?
Can you do this
Now draw a 2nd drug of higher affinity
Can you do this
Can you do this
Can you do this
Can you do this
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
In clinical use of drug we don’t give patient one range, only one dose. We give range in pharmacol expt to see the property of the drug. If give more drug will not increase response cos every system has a max, like you cannot increase HR to 1 million beat per min, and cannot make car go faster when at max speed by putting more petrol (need to change engine). Does not mean higher affinity drug give more response- affinity is binding, response is how you change shape of receptor after bind.
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!!
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Now effect- not binding (lab science)- in ward interested in effect, so from here can’t tell Kd or affinity.
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!!
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Now effect- not binding (lab science)- in ward interested in effect, so from here can’t tell Kd or affinity.
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!!
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Now effect- not binding (lab science)- in ward interested in effect, so from here can’t tell Kd or affinity.
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted. Most-seen graph in pharmacology? (DE or dose response curve). Can you tell the Kd ? No!!
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc
Now effect- not binding (lab science)- in ward interested in effect, so from here can’t tell Kd or affinity.
I like to call dose
Most useful graph to compare different drugs. Most impt graph type in pharmacology.
Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase.
Name of shape: sigmoidal not rect hyperbola
Most useful graph to compare different drugs. Most impt graph type in pharmacology.
Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase.
Name of shape: sigmoidal not rect hyperbola
The units of EC50 and [D] are concentration, but log[D] is unitless.
Most useful graph to compare different drugs. Most impt graph type in pharmacology.
Dose is on log scale. Just plot on this scale give you log value, no need take log and antilog. Scale is log: see the exponential increase.
Name of shape: sigmoidal not rect hyperbola
Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT.
Small dose not compressed together, large dose not flat plateau
Linear middle segment
Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT.
Small dose not compressed together, large dose not flat plateau
Linear middle segment
Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT.
Small dose not compressed together, large dose not flat plateau
Linear middle segment
Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT.
Small dose not compressed together, large dose not flat plateau
Linear middle segment
Most useful graph to compare different drugs. Most impt graph type in pharmacology. We are INTERESTED IN WHAT THE DRUG CAN DO IN THE RANGE OF 20-80% OF MAX EFFECT. OTHER SECTION LESS RELEVANT.
Small dose not compressed together, large dose not flat plateau
Linear middle segment
Kd = EC50 if there is 1:1 relationship bet binding and effect. Usually: full effect with less than full binding- effect is left shifted.
or ED50
Notice Y axis is effect, not binding. Can be any effect measured eg heartbeat, muscle contraction, speed of running, cellular: release of calcium, etc